1,720,965 research outputs found
Mre11 and Ku regulation of double-strand break repair by gene conversion and break-induced replication.
No full text
Going Beyond Counting First Authors in Author Co-citation Analysis
Get PDFThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Variations on the Author
Get PDF“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Appropriate Similarity Measures for Author Cocitation Analysis
Get PDFWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
Dispelling the Myths Behind First-author Citation Counts
Get PDFWe conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation
counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more
sophisticated methods
koamabayili/VECTRON-author-checklist: VECTRON author checklist
No full textWe have done our best to complete the author checklist relating to the use of animals in the hut study. Note that the objective for the hut study was to evaluate the IRS treatment applications for residual efficacy against Anopheles mosquitoes, including the local An. coluzzii mosquito population. Cows were only used to attract mosquitoes into the huts and no tests were carried out directly on the cows. The author checklist is intended for use with studies where experiments are carried out on animals, which is why we have had such difficulty in completing this for the hut study, as many of the questions do not relate to how the cows were used
Regulation of N-formyl peptide receptor trafficking and signaling by arrestins
No full textThis work focuses on how arrestin regulates trafficking and signaling of the N-formyl peptide receptor (FPR), a G protein-coupled receptor (GPCR). GPCRs are involved in almost all physiologic processes and numerous pathologic processes. There is an intimate relationship between GPCR trafficking and signaling that controls many cellular processes. However, the protein-protein interactions that control post-endocytic trafficking and signaling of GPCRs are poorly understood.
Our previous reports demonstrated that three events take place upon FPR activation in the absence of arrestins: accumulation of FPR in the perinuclear recycling endosome, lack of FPR recycling and apoptosis. All of these phenotypes were rescued by reintroduction of arrestin-2 cDNA. We therefore hypothesized that 1) FPR trafficking and signaling defects were linked and causal and 2) specific regions of arrestin-2 regulate normal FPR trafficking and signaling.
To address these hypotheses, we generated mutants of arrestin-2 that were previously described or changed regions of similar amino acids to alanine. We then screened these mutants for the ability to rescue FPR-mediated apoptosis. Subsequently, we examined the role of these arrestin mutants in FPR trafficking. We found that two arrestin-2 mutants demonstrated altered binding to adaptor protein (AP)-2. Furthermore, FPR recycling was inhibited in the presence of either arrestin-2 mutant or the absence of AP-2. We also examined the role of Src kinase in FPR trafficking and signaling and determined that Src kinase has two independent roles in FPR-arrestin-2 regulation: one that controls FPR trafficking and one that mediated FPR signaling. Finally, we found that different SH3-binding domains of arrestin-2 regulate FPR trafficking and signaling independently. An arrestin-2 mutant did not rescue FPR-mediated apoptosis, but did mediate normal FPR trafficking. These results indicate that FPR trafficking and signaling are coordinated processes, but may also be regulated independently.
These studies have revealed novel aspects of arrestin-2 that regulate FPR signaling and trafficking. We hope they will serve as a model for the regulation of other GPCRs. Furthermore, we hope these data are used to create small molecule inhibitors to serve as experimental tools and chemotherapeutics to better understand and treat diseases caused by defects in GPCR trafficking and signaling.Doctor of Philosophy in Biomedical SciencesDoctoralUniversity of New Mexico. Biomedical Sciences Graduate Program.Prossnitz, EricSklar, LarryHudson, LuarieHathaway, Hele
Regulation of N-formyl peptide receptor trafficking and signaling by arrestins
Get PDFThis work focuses on how arrestin regulates trafficking and signaling of the N-formyl peptide receptor (FPR), a G protein-coupled receptor (GPCR). GPCRs are involved in almost all physiologic processes and numerous pathologic processes. There is an intimate relationship between GPCR trafficking and signaling that controls many cellular processes. However, the protein-protein interactions that control post-endocytic trafficking and signaling of GPCRs are poorly understood. Our previous reports demonstrated that three events take place upon FPR activation in the absence of arrestins: accumulation of FPR in the perinuclear recycling endosome, lack of FPR recycling and apoptosis. All of these phenotypes were rescued by reintroduction of arrestin-2 cDNA. We therefore hypothesized that 1) FPR trafficking and signaling defects were linked and causal and 2) specific regions of arrestin-2 regulate normal FPR trafficking and signaling. To address these hypotheses, we generated mutants of arrestin-2 that were previously described or changed regions of similar amino acids to alanine. We then screened these mutants for the ability to rescue FPR-mediated apoptosis. Subsequently, we examined the role of these arrestin mutants in FPR trafficking. We found that two arrestin-2 mutants demonstrated altered binding to adaptor protein (AP)-2. Furthermore, FPR recycling was inhibited in the presence of either arrestin-2 mutant or the absence of AP-2. We also examined the role of Src kinase in FPR trafficking and signaling and determined that Src kinase has two independent roles in FPR-arrestin-2 regulation: one that controls FPR trafficking and one that mediated FPR signaling. Finally, we found that different SH3-binding domains of arrestin-2 regulate FPR trafficking and signaling independently. An arrestin-2 mutant did not rescue FPR-mediated apoptosis, but did mediate normal FPR trafficking. These results indicate that FPR trafficking and signaling are coordinated processes, but may also be regulated independently. These studies have revealed novel aspects of arrestin-2 that regulate FPR signaling and trafficking. We hope they will serve as a model for the regulation of other GPCRs. Furthermore, we hope these data are used to create small molecule inhibitors to serve as experimental tools and chemotherapeutics to better understand and treat diseases caused by defects in GPCR trafficking and signaling
- …
